Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1 (5-Year IF – 2.0)
Journal Citation Indicator (JCI) (2023) – 0.4
Scopus CiteScore – 3.7 (CiteScore Tracker 3.8)
Index Copernicus  – 171.00; MNiSW – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

Download original text (EN)

Advances in Clinical and Experimental Medicine

2018, vol. 27, nr 11, November, p. 1515–1520

doi: 10.17219/acem/70226

Publication type: original article

Language: English

Download citation:

  • BIBTEX (JabRef, Mendeley)
  • RIS (Papers, Reference Manager, RefWorks, Zotero)

Obesity without comorbidity may also lead to non-thyroidal illness syndrome

Şakir Ö. Keşkek1,A,C,D,E,F, Özlem Kurşun1,A,B, Gülay Ortoğlu1,B,E, Mehmet Bankir=1,A,E, Zeynep Tüzün1,B, Tayyibe Saler1,D,F

1 Department of Internal Medicine, Numune Training and Research Hospital, Adana, Turkey

Abstract

Background. Obesity mediates a series of operations in the body by increasing the production of proinflammatory cytokines. Cytokines play an important role in the development of non-thyroidal illness syndrome (NTIS).
Objectives. The aim of this study was to investigate the association between obesity and NTIS.
Material and Methods. A total of 423 subjects were included. The study group was comprised of 219 obese patients without any comorbid disease and the control group was comprised of 204 healthy subjects. Body mass index (BMI), thyroid hormone levels, high-sensitivity C-reactive protein (hs-CRP) levels, erythrocyte sedimentation rate (ESR), complete blood count, and other biochemical parameters were measured. Frequencies of NTIS were calculated. MedCalc 12.5 software program (MedCalc, Ostend, Belgium) was used for statistical analysis.
Results. Groups were statistically different according to BMI (p < 0.001). The mean BMIs of the study and the control group were 34.6 ±5.0 kg/m2 and 22.6 ±1.8 kg/m2, respectively. Obese patients had higher serum hs-CRP levels, ESR and white blood cells (WBC) levels (0.99 ±3.17 mg/L vs 0.39 ±1.09 mg/L; 17.2 ±10.6 mm/h vs 12.6 ±8.0 mm/h; 7.8 ±2.1 103/μL vs 6.9 ±1.5 103/μL, respectively; p < 0.001). There were 21 (9.5%) obese patients with NTIS, while there were none NTIS cases in the control group. The difference was statistically significant (p < 0.001). There was a strong association between obesity and NTIS (odds ratio (OR) = 44.2, confidence interval (CI) = 95% 2.66–736.3; p = 0.0082).
Conclusion. Inflammation, which is strongly associated with adipose tissue, may lead to NTIS in obese patients without any comorbid disease.

Key words

obesity, high-sensitivity C-reactive protein, erythrocyte sedimentation rate, white blood cell, non-thyroidal illness syndrome

References (30)

  1. World Health Organization. Obesity and overweight. http://www.who.int/mediacentre/factsheets/fs311/en//. Accessed December 2, 2017.
  2. Visscher TL, Seidell JC. The public health impact of obesity. Annu Rev Public Health. 2001;22:355–375.
  3. Rippey FF. Thrombosis and embolism. In: General Pathology. Johannesburg, South Africa: Witwatersrand University Press; 2003:103–109.
  4. Rang HP, Dale MM, Ritter JM, Moore PK. Pharmacology. New Delhi, India: Churchill Livingstone; 2006:394–403.
  5. Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman BM. Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest. 1995;95(5):2409–2415. doi: 10.1172/JCI117936
  6. Mathieu P, Poirier P, Pibarot P, Lemieux I, Després JP. Visceral obesity: The link among inflammation, hypertension, and cardiovascular disease. Hypertension. 2009;53(4):577–584.
  7. Hotamisligil GS. Role of endoplasmic reticulum stress and c-Jun NH2-terminal kinase pathways in inflammation and origin of obesity and diabetes. Diabetes. 2005;54(Suppl 2):S73–S78.
  8. De Groot LJ. Non-thyroidal illness syndrome is a manifestation of hypothalamic-pituitary dysfunction, and in view of current evidence, should be treated with appropriate replacement therapies. Crit Care Clin. 2006;22(1):57–86.
  9. Adler SM, Wartofsky L. The nonthyroidal illness syndrome. Endocrinol Metab Clin North Am. 2007;36(3):657–672.
  10. Demers LM, Spencer C. The thyroid. Pathophysiology and thyroid testing. In: Burtis CA, Ashwood ER, Bruns DE, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 4th ed. St. Louis, MO: Elsevier; 2006.
  11. McIver B, Gorman CA. Euthyroid sick syndrome: An overview. Thyroid. 1997;7(1):125−132.
  12. Flegal KM, Graubard BI, Williamson DF, Gail M. Cause-specific excess deaths associated with underweight, overweight, and obesity. JAMA. 2007;298(17):2028–2037.
  13. Mohamed-Ali V, Goodrick S, Rawesh A, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-alpha, in vivo. J Clin Endocrinol Metab. 1997;82(12):4196–4200.
  14. Fried SK, Bunkin DA, Greenberg AS. Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: Depot difference and regulation by glucocorticoid. J Clin Endocrinol Metab. 1998;83(3):847–850.
  15. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris T. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999; 282(22):2131–2135.
  16. Ramírez Alvarado MM, Sánchez Roitz C. Relation of serum levels of C-reactive protein to anthropometric measurements: A systematic review of studies in South America [in Spanish]. Nutr Hosp. 2012;27(4):971−977.
  17. Bartalena L, Brogioni S, Grasso L, Velluzzi F, Martino E. Relationship of the increased serum interleukin-6 concentration to changes of thyroid function in nonthyroidal illness. J Endocrinol Invest. 1994; 17(4):269−274.
  18. Boelen A, Platvoet-Ter Schiphorst MC, Wiersinga WM. Association between serum interleukin-6 and serum 3,5,3’-triiodothyronine in nonthyroidal illness. J Clin Endocrinol Metab. 1993;77(6):1695–1699.
  19. Davies PH, Black EG, Sheppard MC, Franklyn JA. Relation between serum interleukin-6 and thyroid hormone concentrations in 270 hospital in-patients with non-thyroidal illness. Clin Endocrinol. 1996;44 (2):199–205.
  20. Rasmussen AK. Cytokine actions on the thyroid gland. Dan Med Bull. 2000;47(2):94–114.
  21. Ozawa M, Sato K, Han DC, Kawakami M, Tsushima T, Shizume K. Effects of tumor necrosis factor-alpha on thyroid hormone metabolism in mice. Endocrinology. 1988;123(3):1461–1467.
  22. van der Poll T, Romijn JA, Wiersinga WM, Sauerwein HP. Tumor necrosis factor: A putative mediator of the sick euthyroid syndrome. J Clin Endocrinol Metab. 1991;71(6):1567–1572.
  23. Hermus AR, Sweep CG. Cytokines and the hypothalamic–pituitary–adrenal axis. J Steroid Biochem Mol Biol. 1990;37(6):867–871.
  24. Tognini S, Marchini F, Dardano A, et al. Non-thyroidal illness syndrome and short-term survival in a hospitalised older population. Age Ageing. 2010;39(1):46−50.
  25. Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor alpha: Direct role in obesity-linked insulin resistance. Science. 1993;259(5091):87–91.
  26. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999;282(22):2131–2135.
  27. Sartipy P, Loskutoff DJ. Monocyte chemoattractant protein 1 in obesity and insulin resistance. Proc Natl Acad Sci U S A. 2003;100(12):7265–7270.
  28. El-Wakkad A, Hassan N-M, Sibaii H, El-Zayat SR. Proinflammatory, anti-inflammatory cytokines and adipokines in students with central obesity. Cytokine. 2013;61(2):682–687.
  29. Menon V, Zhi X, Hossain T, et al. The contribution of visceral fat to improved insulin signaling in Ames dwarf mice. Aging Cell. 2014;13(3): 497−506.
  30. Masternak MM, Bartke A, Wang F, et al. Metabolic effects of intra-abdominal fat in GHRKO mice. Aging Cell. 2012;11(1):73−81.
© Wroclaw Medical University